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Study · Measured the body's own peptide · 2015

6 results

Thymosin Beta-4, Actin-Sequestering Protein Regulates Vascular Endothelial Growth Factor Expression via Hypoxia-Inducible Nitric Oxide Production in HeLa Cervical Cancer Cells.

Ryu YK, Lee JW, Moon EY

Biomolecules & therapeutics1 Jan 2015Cited by 16 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC. Results still quote short attributed sentences.

Results from this study6

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01LabEndogenous levelIn vitro (cells)Mechanism

    In hypoxic HeLa cells, the NOS inhibitor L-NMMA lowered expression of the body's own Tβ4.

    In plain wordsIn cells under low oxygen, a drug that blocks nitric oxide synthase lowered the cells' own Tβ4.

    Outcome
    DecreaseTβ4 expression after NOS inhibition in hypoxia
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    In hypoxic condition, HRE-luciferase activity and VEGF expression were inhibited by the treatment with N(G)-monomethyl-L-arginine (L-NMMA), an inhibitor to nitric oxide synthase (NOS), which is accompanied with a decrease in Tβ4 expression.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone5

In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Thymosin beta-4 (human).

  1. 02LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In HeLa cells, Tβ4 siRNA knockdown reduced hypoxia-inducible nitric oxide production.

    In plain wordsIn cells, lowering the cells' own Tβ4 reduced nitric oxide production under low oxygen.

    Outcome
    DecreaseHypoxia-inducible NO production after Tβ4 knockdown
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Hypoxia inducible NO production and VEGF expression were reduced by small interference (si) RNA of Tβ4.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

  2. 03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In HeLa cells, Tβ4 siRNA knockdown reduced hypoxia-inducible VEGF expression.

    In plain wordsIn cells, lowering the cells' own Tβ4 reduced VEGF levels under low oxygen.

    Outcome
    DecreaseVEGF expression after Tβ4 knockdown
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Hypoxia inducible NO production and VEGF expression were reduced by small interference (si) RNA of Tβ4.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

  3. 04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In HeLa cells, Tβ4 siRNA inhibited the rise in HRE-luciferase activity caused by the NO donor SNAP-1.

    In plain wordsIn cells, lowering the cells' own Tβ4 blocked the rise in HRE-luciferase activity caused by a nitric oxide donor.

    Outcome
    DecreaseNO-induced HRE-luciferase activity after Tβ4 knockdown
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Hypoxia response element (HRE)-luciferase activity and VEGF expression were increased by the treatment with N-(β-D-Glucopyranosyl)-N2-acetyl-S-nitroso-D, L-penicillaminamide (SNAP-1), to generate NO, which was inhibited by the inhibition of Tβ4 expression with Tβ4-siRNA.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

  4. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In HeLa cells, Tβ4 siRNA inhibited the rise in VEGF expression caused by the NO donor SNAP-1.

    In plain wordsIn cells, lowering the cells' own Tβ4 blocked the rise in VEGF caused by a nitric oxide donor.

    Outcome
    DecreaseNO-induced VEGF expression after Tβ4 knockdown
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Hypoxia response element (HRE)-luciferase activity and VEGF expression were increased by the treatment with N-(β-D-Glucopyranosyl)-N2-acetyl-S-nitroso-D, L-penicillaminamide (SNAP-1), to generate NO, which was inhibited by the inhibition of Tβ4 expression with Tβ4-siRNA.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

  5. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In HeLa cells treated with L-NMMA, Tβ4 overexpression from a plasmid restored VEGF expression.

    In plain wordsIn cells, extra Tβ4 from a plasmid brought back VEGF levels that a nitric oxide synthase blocker had lowered.

    Outcome
    IncreaseVEGF expression restored by Tβ4 overexpression after L-NMMA
    Study

    humann: not reported in source

    HeLa cervical cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    VEGF expression inhibited by L-NMMA treatment was restored by the transfection with pCMV-Tβ4 plasmids for Tβ4 overexpression.
    1 context sentence
    Summary · context
    Here, we investigated whether NO-mediated VEGF expression could be regulated by Tβ4 expression in HeLa cervical cancer cells.

    In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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